Department of Pathology, University of Texas Southwestern Medical Center, Dallas, USA.
Adv Chronic Kidney Dis. 2011 Mar;18(2):91-7. doi: 10.1053/j.ackd.2010.11.007.
Phosphorus is an essential nutrient and is routinely assimilated through consumption of food. The body's need of phosphate is usually fulfilled by intestinal absorption of this element from the consumed food, whereas its serum level is tightly regulated by renal excretion or reabsorption. Sodium-dependent phosphate transporters, located in the luminal side of the proximal tubular epithelial cells, have a molecular control on renal phosphate excretion and reabsorption. The systemic regulation of phosphate metabolism is a complex multiorgan process, and the identification of fibroblast growth factor-23 (FGF23)-Klotho system as a potent phosphatonin has provided new mechanistic insights into the homeostatic control of phosphate. Hypophosphatemia as a result of an increase in urinary phosphate wasting after activation of the FGF23-Klotho system is a common phenomenon, observed in both animal and human studies, whereas suppression of the FGF23-Klotho system leads to the development of hyperphosphatemia. This article will briefly summarize how delicate interactions of the FGF23-klotho system can regulate systemic phosphate homeostasis.
磷是一种必需的营养物质，通常通过食物摄入来吸收。人体对磷酸盐的需求通常通过肠道从所摄入的食物中吸收这种元素来满足，而其血清水平则由肾脏排泄或重吸收来严格调节。位于近端肾小管上皮细胞腔侧的钠依赖性磷酸盐转运体对肾脏磷酸盐的排泄和重吸收具有分子控制作用。磷酸盐代谢的全身调节是一个复杂的多器官过程，成纤维细胞生长因子 23（FGF23）-Klotho 系统作为一种有效的磷酸盐激素的发现，为磷酸盐的体内平衡控制提供了新的机制见解。FGF23-Klotho 系统激活后尿磷酸盐排泄增加导致的低磷酸盐血症是一种常见现象，在动物和人类研究中均有观察到，而 FGF23-Klotho 系统的抑制则会导致高磷酸盐血症的发生。本文将简要总结 FGF23-Klotho 系统的精细相互作用如何调节全身磷酸盐的体内平衡。
